CVS MMF S7-12 Flashcards
causes of tachycardic arrhythmias
ectopic pacemaker activity
- damaged myocardium
- pacemaker region activated from ischaemia (damaged myocardium doesn’t conduct well so spontaneously generates own AP)
Afterdepolarisations
Atrial flutter
Re-entry loops
- conduction delay
- accessory pathway (WPW)
causes of bradycardia arrhythmias
sinus Brady
- intrinsic SAN dysfunction
- extrinsic factors e.g. drugs
conduction block
- problem at AVN/ bundle of His (R/LBBB)
- slowed conduction at AVN due to drugs
which is worse VF or AF
AF
treat AF so it doesn’t turn to VF > harder to treat VF
example of re-entry loop condition and its presentations
wolf parkinson white
- congenital accessory pathway
- atrioventricular re-entrant tachycardia
> pre excitation of vessels
give an example of when re-entry loop can occur
post MI due to damaged tissue
instead of excitation spreading in a loop in opposite directions then cancelling out, one will be blocked and then the other will re-circulate causing arrhythmia
what are class 1 anti-arrythmics
1B
Na+ channel blockers
- slows conduction in phase 0
- slows Na entry, slows upstroke > stops new impulse arising as channels blocked
dec ARP. and dec AP duration.
e.g. lidocaine. fast acting!!
what are class 2 anti-arrythmics
Beta blockers
inhibit sympathetic action on. heart
decreases adrenaline action on B1 adrenoreceptors, less Ca entry into cell, reduced contraction. lowers HR
at pacemaker cells: slows upstroke of funny current (phase4)
no pacemaker cells: low Ca entry, longer plateau in phase 3> longer ARP >dec re entry of arrhythmia
e.g. attenalol
problem with beta blockers in asthmatics?
some aren’t cardio selective and can work on B1 too causing bronchospasms
what are class 3 anti-arrythmics
K+ channel blockers
> prolong ARP and AP duration
prevents another AP from occurring
e.g. amiodarone multi class effects> dec conduction across all cardiac tissue
problem with K+ channel blockers?
can easily devolve and produce early after depolarisations > develop into VT
which drugs can also have a pro-arrhythmic effect?
any drug that prolongs cardiac AP> prolongs QT interval
class 3!!
why do early after depolarisations occur
reactivation of Ca channels
why do delayed after depolarisations occur
abnormally increased intracellular Ca
hypercalcemia or hypokalaemia
what is digoxin toxicity
class 5 drug
lead to an overload. of Ca into SR
spontaneous Ca release
net depolarisation effect
> delayed afterdepolarisations occur
what are class 4 anti-arrythmics
Ca channel blockers
pacemaker cells:slower Ca entry, shallow upstroke, slow HR
inc ARP
non: slow Ca entry, dip in plateau phase> dec contractility
dec HR and inotropy!!
e.g. verapamil
what are class 5 anti-arrythmics
positive inotropes
Digoxin - cardiac glycoside
Dobutamine- Beta agonist
How does digoxin work?
enhances vagal activity
lower HR and slows conduction through AVN > inc diastolic filling time
Blocks Na/K ATPase, inc intracellular Na, dec activity of NCX> more Ca stored in SR
> contractility increases
how does dobutamine work
stimulates B1 adrenoreceptors at SAN and AVN
steeper funny current > HR inc
contractility inc
in what locations do you take pulses from in the lower limb
femoral area
popliteal area
tibialis posterior area
dorsalis pedis area
what is intermittent claudication
peripheral vascular disease> causes arterial insufficiency due to atherosclerosis in vessels
- cramping pain
- relieved by rest
- pain that’s reproducible
what are the signs associated with acute limb ischaemia?
6Ps
- pallor
- pain
- perishing with cold
- paraesthesia
- paralysis /reduced power
- pulselessness
stages of atherosclerosis formation?
repeated injury to endothelium
tunica intima becomes permeable to LDL/ lipoproteins
macrophage migration. to endothelial wall
macrophages absorb LDL> form foam cells
further inflammatory mediators enter
platelets aggregate and adhere to foam cells
smooth muscle cells migrate to surface of plaque > fibrous plaque formation
difference between stable and unstable angina?
stable- ischaemia that happens when metabolic demand increases e.g.during exercise >symptoms don’t last long. relieved with rest
unstable-pain doesn’t resolve
usually more painful.
treatment for angina how does it work?
beta blockers
ca blockers
GTN spray>venodilator > decpreload on heart > dec isotropy. > muscle doesn’t. have to contract as hard so doesn’t require as much oxygen
diff between NSTEMI and STEMI
NSTEMI
- ST depression
- partial occlusion, reduced perfusion
STEMI
- ST elevation
- full thickness, complete occlusion
how to differentiate between NSTEMI and unstable angina
troponin test
I and T
> indicates myocyte damage in NSTEMI
what is the ECG progression of a stemi
hyper acute T waves (wide and tall)
ST elevation
inverted T waves
pathological Q waves
causes of peripheral oedema?
3Ps
physiological- heat> leaky vessels or pregnancy vasodilation
pharmacological-calcium channel blockers or IV fluids
physiological- cardiovascular , liver, renal
causes of left sided HF
caused by pressure overload from long term hypertension or valve dysfunction (aortic stenosis)
volume overload >valve regard
myocardium dysfunction >ishcaemic HD
causes of right sided HF
LHF
backup of blood through the pulmonary system > RV pushing against higher pressure > ventricular hypertrophy > eventually RHF
what is Cor pulmonale
RHF from pulmonary hypertension
what is diastolic dysfunction in HF?
ventricles still can relax normally > cant fill as much >blood backs up to lungs > ventricular muscle hypertrophies > wall thickens
what is systolic dysfunction in HF?
IHD/HTN > chambers of heart enlarge >walls thin > overstretches sarcomeres in muscle>prevent efficient contractions > less blood pumped out
what is ejection fraction
amount of blood pumped out the ventricles over the total amount of blood in ventricles
normal= 50%ish
reduced ejection fraction?
<40%
seen in systolic dysfunction (increased volume in but less pushed out)
diastolic dysfunction ejection fraction?
preserved>smaller volume in but ventricular contraction not compromised
describe the RAAS in relation to heart failure
HF> reduced CO > reduced blood flow to kidneys > renin released > angiotensinogen converted into Ang-1> ACE converts Ang 1 to Ang 2
> causes vasoconstriction> inc afterload
> causes inc Na and water reabsorption > inc intravascular volume >inc pre load !!
what is preload
volume of blood entering right side of heart
afterload?
resistance that the LV must overcome to push blood out
what is cariogenic shock?
when heart cannot maintain CO (pump failure) > tissues poorly perfused >ishcaemia > organ failure
e.g. MI/ dilated cardiomyopathy/ heart failure
types of shock
distributive
hypovolaemic
cariogenic
mechanical
> > all produce reduction in BP>tissue ishcaemia > multi organ failure
do this by dec TPR or CO
effect of ACE inhibitors
reduced ADH and aldosterone release. These both reduce blood pressure.
mechanism of action of diuretics
act to lower the preload and afterload to decrease the load on the heart, and also to increase fluid loss to lower blood pressure.
initial pharmacological therapy for heart failure patient
ACE inhibitor ARBs (angiotensin receptor blockers) diuretics beta blockers aldosterone receptor antagonist (spironolactone)
RAAS system activation causes
- Increased sodium retention leading to increased water retention
- Increased ADH release
- Vasoconstriction
- Enhances Sympathetic activity
> all inc BP!!
mitral stenosis effect on pulmonary capillary pressure ?
- inc pulmonary capillary pressure
bc the left atrial pressure increase, which will increase the capillary pressure in the lungs.
